1. Field of the Invention
The present invention relates to sleep optimization, and more particularly to providing a system for optimizing an individual's time spent sleeping, for providing a uniquely timed wake up alert to minimize the pitfalls of sleep inertia, to leave the individual feeling energized, and to entrain the individual's circadian rhythm.
2. General Background
The physiological phenomenon of human sleep is heterogeneous in nature, and its great variation is influenced heavily by factors outside the body. As part of understanding sleep and what affects it, a great deal of research has generally agreed that sleep can be broken down into two broad types: Rapid Eye Movement (REM) and Non-Rapid Eye Movement (NREM). NREM is subdivided into light sleep, which consists of Stage 1 and Stage 2 sleep, and slow wave sleep (SWS, also known as “deep sleep” or “delta sleep”), which consists of Stage 3 and Stage 4 (some researchers no longer divide SWS into Stage 3 and Stage 4, and instead treat it as a single stage). As the above named stages imply, NREM sleep comprises four successively deeper stages of sleep—Stages 1 through 4. While sleeping, humans cycle through the above stages, as shown best in FIG. 1. A typical sleep cycle begins with the transition from waking to Stage 1 sleep and then progresses through Stage 2, Stage 3, and finally Stage 4 before returning back through Stage 3 to Stage 2. Rather than progressing all the way back to Stage 1 sleep, at this time the typical sleep cycle enters REM sleep (sometimes with a transitory pass through Stage 1 sleep). Stage 4 can be seen in FIG. 1 just above the 1-hour mark, and the transition back to the lighter stages is seen immediately thereafter. Upon the conclusion of REM sleep, the typical sleep cycle progresses back to Stage 2 (also sometimes with a transitory pass through Stage 1) and on to Stage 3 and Stage 4 and then back through Stage 3 and Stage 2 at which time the cycle again enters REM sleep (again, possibly with a transitory pass through Stage 1) and repeats. While there is significant variability among individuals, the typical sleep cycle duration is about 90 minutes. The percentage of the cycle spent in REM increases as the night progresses while the percentage of cycle time spent in SWS decreases.
There are numerous physiological differences between REM sleep and NREM sleep. REM sleep is characterized by rapid eye movement, muscular atonia, dream content, fluctuations in autonomic function (irregular respiration, pulse, temperature, and blood pressure), a brain metabolic rate similar to waking, and desynchronized neuronal activity. There is neither noradrenergic activity nor serotonergic activity during REM. By comparison, NREM sleep is characterized by relatively little eye movement, muscle tone, little dream content, regular pulse, temperature, and blood pressure, relatively low brain metabolic rate, and synchronized neuronal activity. Further, in NREM increased tissue synthesis, cell division, and growth hormone release is observed relative to waking or REM stages. Many of these physiological differences can be monitored non-invasively so as to distinguish between REM and NREM sleep.
While there is still much to be learned about sleep, there are a few theories (not necessarily mutually exclusive) that have gained merit regarding the question “why do we sleep.” The “adaptive theory” argues that sleep functions to increases the probability of an animal's survival (feeding, other predatory behavior, and avoiding danger). Support for this theory stems from the observation that sleep-wake patterns differ within species and are well suited for the species particular biological niche. The “Energy Conservation Theory” instead focuses on the idea that the reduced metabolic rate during sleep helps retain energy. Generally animals with high metabolic rates sleep longer than animals with slower metabolic rates. For the purposes of this discussion, however, we are most concerned with the widely accepted “Restorative Theory of Sleep,” in which the general implication is that sleep plays an important role in revitalization.
Mechanisms underlying the restoration process include neutralization of neurotoxins that accumulate during waking hours, responses to increased sleep-inducing substances that are produced during waking processes, neurochemical synthesis, and brain chemical redistribution. During SWS, increased tissue synthesis, cell division, and growth hormone release is observed. Athletes have higher proportions of SWS than others. Oxygen consumption declines during SWS suggesting reduced catabolism. SWS increases after starvation in an apparent compensatory effect. Hyperthyroidism increases SWS whereas hypothyroidism reduces SWS, and SWS is high during peak physical developmental years in children and declines during advancing age. Last, research indicates that SWS has an intensity component. This intensity dimension of SWS apparently allows mammals to compensate for lost sleep without having to significantly increase sleep time. It is important to note, however, that is unclear if such an intensity dimension exists for REM sleep and thus it may be more difficult to compensate for lost REM sleep.
While NREM sleep, and in particular SWS appear to play a central role in physical restoration the purpose of REM sleep seems to be different. Although the current state of research does not support definitive answers, there are numerous compelling hypotheses regarding the purpose of REM sleep. Understanding the differences between REM and NREM sleep is key to the ensuing discussion and conclusions.
The lower metabolic rates and lower body temperatures of NREM apparently provide an environment conducive to neuronal repair. REM sleep does not serve the same purpose (neuronal activity is similar to that of waking activity), but it may serve yet another role: the restoring full sensitivity of monoamine receptors (especially those for norepinephrine, serotonin and histamine). This is accomplished by the cessation of monoamine neurotransmitter release during REM sleep (causing sleep paralysis and reducing environmental awareness).
Furthermore, the “Programming-reprogramming Hypothesis” claims that sleep (specifically REM sleep) serves to remove unimportant information and consolidates and strengths more important experiences. Evidence includes the fact that infants, whose brains are presumably experiencing significant change during development, sleep twice as much as adults, and much of this time is spent in REM. Other theories related to this hypothesis argue that REM sleep is important in memory (especially memory consolidation) and intellectual function. Studies show that REM sleep increases during intense learning experiences and that REM sleep deprivation leads to reduced creative problem solving ability. Experiments have shown that perceptual skills, such as those that are learned through repeated practice, improve overnight and are disrupted if there is selective interruption of REM sleep. Other experimental data suggest that cerebral activation that occurs during REM sleep plays a key role in brain development.
REM sleep is additionally linked to proper functioning of active growth and development of the nervous system. The fact that REM sleep is resistant to age-related changes is believed to suggest a role in maintaining nervous system function. Moreover, while the purpose of dreaming (a key distinguishing feature of REM) is even less well understood than REM, many the theories about it reinforce the cognitive-health importance of REM sleep. These theories include proposing that dreaming (and thus REM) is intertwined with long-term memory consolidation of semantic memories, learning, and resolution of distressing experiences.
Of particular interest to those hoping to wake cognitively alert is yet another possible function of REM sleep. Mammals experience much more REM sleep than do reptiles. This may be related to the cold-blooded and slow-awaking nature of reptiles as opposed to the relative quick start of mammals. In this context, REM sleep is seen as a way for mammals to become alert quickly through REM-priming. That is to say that during REM sleep, relative to the other states of sleep, the brain is functioning most like its waking state, and thus the transition from sleeping to waking requires relatively little adjustment. By comparison, in Stage 2 the brain does not function like its waking state. In Stages 3 or 4 the brain functions even less like its waking state. The deeper the sleep (with Stage 1/REM being the lightest and Stage 4 being the deepest) the more dissimilar the brain's activity is relative to waking brain activity, with a pronounced difference between light NREM and SWS NREM (making the Stage 2/Stage 3 transition of particular importance in certain cases).
A phenomenon related to the transition from sleeping to waking that is key to our discussion is that of “sleep inertia” (also known as sleep drunkenness). It is a phenomenon that normally occurs in humans during the transition from sleep to wakefulness, and refers to a period of impaired performance (both cognitive and motor), reduced vigilance, general grogginess, disorientation, a propensity to want to return to sleep, etc. The impairment may be severe and may last anywhere from minutes to several hours. Studies have scientifically demonstrated the debilitating effects of sleep inertia, and have found the average duration to be between 1 and 3 hours depending on the time of waking (night wake ups lead to longer durations). The impaired performance attributable to sleep inertia has important implications for many activities, especially those that require rapid decision making following forced abrupt awakenings (for instance, an on-call doctor sleeping at a hospital) or for activities following naps.
While the cause of sleep inertia is still unknown (not to say that there are no theories), there are some key factors that seem to play a role in influencing the potency of the effect. One of the main factors is thought to be the depth of the sleep at the time of waking; the deeper the sleep the worse the sleep inertia. While the reason for this correlation is unknown, there is reason to believe that it is related to the difference in brain function during stages 1 through 4 relative to waking, and the related REM-priming discussed earlier. The difference between light NREM and deep (SWS) NREM is then of particular importance to determining the effect of sleep inertia because SWS NREM brain activity contrasts starkly with waking activity. This is not to say that Stage 1 and Stage 2 activity are similar to waking activity, rather it highlights the transition from light to deep sleep (and the resulting sleep inertia effects) as being more abrupt than one might expect; a few minutes difference in wake time relative to the sleep cycle can significantly affect the strength of the sleep inertia. It is from this understanding of sleep inertia that some suggest the best nap is a brief one (10 to 30 minutes). The idea is that the subject wakes before entering SWS, which generally occurs a little more than 30 minutes into the sleep cycle.
Another factor which influences sleep inertia is the timing of the sleep. Studies have shown that more sleep inertia results when waking near a trough in the body temperature (which cycles throughout the day). By contrast, subjects often experience less sleep inertia when waking near a body temperature high.
The body's temperature cycle is directly related to the phase of the circadian rhythm (the body's natural daily rhythm). Under proper conditions, the body temperature cycle, the circadian rhythm, and the sleep-wake cycle stay relatively consistent (generally the body temperature nadir occurs between the third sleep cycle and approximately two hours before the subjective wake time). The phase of the sleep-wake cycle is able to shift more rapidly than the circadian rhythm phase (and its underlying body temperature cycle), which can result in the minimum body temperature occurring at different times relative to the subjective wake time. Jet lag is the result of a significant shift between the sleep-wake cycle and the circadian rhythm. Shift work can also lead to the two cycles falling out of synchronization. The changing environment can also play a role, especially in cases such as Seasonal Affective Disorder (SAD). Disruption of the thermoregulation and sleep-wake cycles may lead to problems both initiating and maintaining sleep, abnormal sleep architecture, and resulting daytime sleepiness.
The human circadian rhythm, when allowed to cycle without outside stimulus, varies from just under 24 hours to more than 27 hours in length with the average falling at about 24.5 hours. Under the influence of outside stimulus, the circadian rhythm can be “entrained” (influenced) in such a way that its duration can be extended or shortened, and its phase shifted relative to other cycles. Of the possible environmental stimuli that can work to “entrain” the circadian rhythm, light is far and away the dominant synchronizer for the circadian pacemaker, including phase shifts. The suprachiasmatic nucleus (SCN) in the anterior hypothalamus, dorsal to the optic chiasm serves as mammals' master pacemaker for circadian rhythms. Photic information is relayed to the SCN via the retinohypothalamic tract. Further, studies have shown that a specific subset of light is particularly effective at resetting the circadian rhythm, specifically blue/green light in the range of 420-500 nm.
Greater light intensity has been shown to produce greater circadian shift. However, equally important in obtaining a desired circadian shift is the timing of the exposure. As noted earlier, when the circadian rhythm is properly synchronized with the sleep-wake cycle the body temperature minimum occurs about five to six hours after usual bedtime (about two hours before usual wake time). The body temperature minimum will stray farther from this synchronized point as disruption of the circadian and sleep-wake cycles becomes greater. Of particular importance to our discussion is that the body temperature minimum is theorized to provide an inflection point which determines the circadian-phase-shift direction caused by light exposure. That is, studies show that light exposure before the temperature nadir delays the circadian phase, extending the day, causing a later wake-up time and later sleep onset. By contrast, light exposure on the dawn side of the temperature nadir (after it occurs) has been show to phase advance the circadian rhythm, causing earlier wake-up and sleep onset.
The so-called “Phase Response Curve” (PRC) illustrates the relationship between the timing of light exposure and the effect on the circadian rhythm. The studies that have led to the PRC indicate that for much of the day, light has little effect on the circadian rhythm. Light begins to have a phase delaying effect about seven hours before the body temperature minimum (about two hours before the usual bedtime). The effect strengthens from a phase-shift of a few minutes to phase-shifts as great as two to three hours as the exposure time gets closer and closer to the body temperature minimum. The PRC peaks just before the temperature minimum at which time the inflection point shows the abrupt change from phase delay to phase advance. Exposure a few minutes before the temperature minimum is theorized to produce the most pronounced phase delay (up to two to three hours) while light exposure a few minutes after the temperature minimum is theorized to produce the most pronounced phased advance (also up to two to three hours). After this abrupt inflection point, light exposure for approximately the four hours following the temperature minimum affect circadian phase advance with the most effective times being closet to the temperature minimum. After these approximately four hours (about two hours after usual wake up time) the phase shift effectiveness again falls to near zero. There is still much to be learned about circadian phase entrainment, but the inflection point created by the body temperature minimum seems to be key.
Given the limited and simplistic nature of existing alarm clocks, for most individuals it is to a large extent chance as to which stage he or she will be in when the alarm clock goes off. It is an all too common occurrence to be awakened while in a deeper sleep stage. When this occurs, it is common for the awakened individual to subsequently suffer the mal effects of sleep inertia, which drastically decrease a person's awareness, effectiveness, and efficiency. There is a clear need for an intelligent system which is capable of monitoring the sleep cycles of its user such that the user can be awakened at the time that best maximizes his or her alertness and energy in a efficient and productive manner.
The manner in which a person is awakened is also important in seeking to optimize alertness and energy. Not only does some research show that gradual awakenings are preferable to abrupt awakenings, but as noted earlier, it is well known that exposure to light when waking, especially light directed at the eyes and other particular parts of the body, are important in resetting the body's circadian rhythm, or “natural clock”, to maximize the alertness and “awake” feeling of the subject. A system that can additionally appropriately entrain the circadian rhythm (whether it be the daily struggle to phase-advance the circadian rhythm from its natural 24-plus hour duration to the earth day's 24 hour cycle or the even more greatly desynchronized jet-lag-suffering or shift-work subject) will prove all the more beneficial to this end. Thus, there is an advantage to waking the user through the use of a simulated sunrise achieved via the ramping up to full brightness a source of illumination.